Diabetes, an abnormal metabolic disease, is induced by a defect in the mechanism of glucose metabolism.
Under normal conditions, glucose metabolism occurs as follows:
Carbohydrates, consumed in t he form of food, are digested to glucose in the intestines prior to absorption into the circulatory system. Pancreatic .beta. cells respond to an increase in the blood glucose level by secreting insulin, which in turn stimulates the target peripheral tissues (muscles and liver) to decrease the blood glucose level by enhancing tissue absorption of the blood glucose followed by conversion to glycogen for storage.
Depending on the causative factors, diabetes is classified into two major categories; insulin dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM). IDDM (Type I diabetes) is a pathological condition where insulin is not secreted or insufficient even on secretion by pancreatic .beta. cells responding to an increase in the blood glucose level induced by food consumption. It has been known that destruction of .beta. cells of the pancreatic islets induces IDDM. The current therapy employs supplementation of insulin from exogenous sources.
NIDDM (Type II diabetes) is a pathological condition where the feedback mechanism of peripheral tissues is dysfunctional and is ineffective in decreasing the blood glucose level although normal insulin secretion occurs within the living system. In the United States of America, NIDDM is said to be a common disease; 5% of the population exceeding 40 years of age suffer from NIDDM. Causative factors involved in this disease have yet to be elucidated.